Antioxidant Defense Systems and Trace Minerals

Posted: February 26, 2021

The amount of scientific research giving strong evidence to support the positive benefits of antioxidant nutritional supplementation continues to grow. Free radicals (antioxidants’ arch enemy) are contributors to diseases and to the aging process and have become popular focal points of clinical research.

Free radicals have been implicated as a major factor in the following health problems: arthritis, atherosclerosis (a common disease caused by cholesterol deposits obstructing blood flow in the arteries), ischemic heart disease (reduced blood supply to the heart muscle), cancers, cataracts, emphysema (a progressive disease of the lungs) and retinopathy (a persistent inflammation or acute damage to the retina of the eye, usually caused by diabetes).

The main target of free radicals is the polyunsaturated fats (PUFA) that make up the major part of the cell membranes. Free radical attacks can cause the PUFAs to undergo a process called peroxidation (becoming rancid). This rancidity causes further free radical damage, which leads to cellular damage, and the beginning of health problems such as those listed above.

Knowledge has grown with respect to the roles of the antioxidant/micronutrients in combatting free radicals. Vitamin E, vitamin C, and beta-carotene (like the orange colored provitamin A found in carrots) are potential weapons against the dangers of free radicals, and they have become the most investigated antioxidants and micronutrients. Research evidence points to their effectiveness in fighting atherosclerosis and cataracts as well as enhancing the immune system.

More recently, the roles of certain trace minerals in the maintenance of the body’s antioxidant defense system have produced increased interest: selenium, iron, copper, zinc, and manganese (a required trace mineral for all living things—not to be confused with magnesium) have all exhibited crucial antioxidant involvement.

What is Superoxide Dismutase (SOD), and what does it do?

A major player in the body’s antioxidant defense system is an enzyme known as superoxide dismutase (SOD). Many supplements reportedly offer SOD as an ingredient. Unfortunately, this SOD ingredient cannot be effectively taken orally because it is destroyed during the digestive process, making SOD supplements of little or no value. Instead, we need to supplement certain components of the SOD so that the body can absorb it.

How do these nutrients aid the SOD defense systems? Scientific studies have shown that the proper intake of copper, zinc, and manganese are required for optimal activity of the several types of SODs. All of the antioxidant protective systems require the presence of specific trace minerals such as these to protect the body.i

Albion’s Approach to SOD (Superoxide Dismutase – the Body’s Antioxidant Defense) System Maintenance

The body’s antioxidant defense system relies on optimal nutritional support of specific nutrients. Vitamin C, beta carotene (like the orange provitamin A found in carrots) and vitamin E are commonly taken to supply the body with key ingredients for its antioxidant defense system. Each of these antioxidants plays a different role in the fight against free radicals. This is why taking just one antioxidant doesn’t do the trick. In addition, the antioxidants from different sources or chemical types have shown varied abilities against free radicals. Some antioxidants have even been shown to have regenerating effects on other antioxidants, such as vitamin C and vitamin E.

As previously covered, due to the size of the SOD enzymes, taking an SOD supplement does nothing, as the enzymes are digested and destroyed in the GI tract.

The best way to fuel the body’s SOD supply is to provide an optimal supply of the individual components, such as: copper, zinc, and manganese amino acid chelates. Several studies involving these patented Albion chelated trace minerals have shown that the use of these highly absorbable chelated trace minerals results in greater SOD activity in the body’s defense system.

Superoxide Dismutase Antioxidant Defense System; Manganese and Iron Status in Women

This study evaluated the changes in SOD activity and manganese and iron status in 47 women during a 124-day supplementation period.

The women received one of four treatments: placebo, 60 mg of iron, 15 mg of manganese, or both mineral supplements. Due to reports of higher bioavailability (absorption of the dose of minerals into the body’s circulatory system) the researchers chose manganese amino acid chelate made by Albion for the study.

Albion’s amino acid chelate form was reported to have an 82.3% greater rate of absorption. Both groups taking the manganese amino acid chelate supplement experienced significant increases in antioxidant defense activity. The group taking the iron supplement alone exhibited the lowest antioxidant defense activity.ii

Copper and Zinc Status of Patients with Coronary Artery Disease (CAD)

Recent evidence has linked oxidative changes in the low density lipoprotein cholesterol (LDL-C) to be associated with the development of atherosclerosis, a disease characterized by cholesterol deposits in the arteries obstructing blood flow. LDL-C enables fats and cholesterol to move within the water-based solution of the bloodstream, and when oxidative changes take place, cholesterol deposits accumulate in the arteries.  However, trace minerals such as copper and zinc are reported to prevent cholesterol deposits in the arteries and have been shown to block the oxidation that can cause atherosclerosis.

In this study, the researchers examined the copper and zinc status of 50 patients admitted to Duke Medical Center for cardiac catheterization, which is the insertion of a catheter into a chamber of the heart for treatments and investigation. Twelve patients had minor coronary artery disease (CAD) while the other 38 had significant CAD.

The patients with significant CAD were found to have low dietary intakes of copper and zinc. The researchers felt that this study suggested that adequate copper status may have a positive influence on LDL-C levels, in addition to the roles that the two trace minerals play in blocking oxidation.iii

Amino Acid Chelates Increase SOD (Superoxide Dismutase – the Body’s Antioxidant Defense System) Activity in Animals

In an animal study conducted at Oklahoma State University, investigators gave a group of cattle a supplement containing copper, manganese, and zinc in the form of Albion’s amino acid chelates (a highly available form of the minerals for absorption into the body). Another group of cattle were given inorganic metal salts, which can be difficult for the body to digest and absorb. They found that when the animals received Albion’s copper, manganese, and zinc chelates, the SOD antioxidant defense system was significantly increased. Over a 60 day period, the SOD antioxidant defense system in the group receiving Albion’s chelates increased 11.7%, whereas the SOD defense system in the group ingesting the inorganic metal salts decreased 3.8%.iv

To illustrate:

Recent Dr. DiSilvestro, at Purdue University, compared 23 people afflicted with rheumatoid arthritis to 48 healthy individuals. People who have rheumatoid arthritis have low copper/zinc SOD activity. The investigators gave the arthritic group 2 mg of copper per day, as Albion’s copper amino acid chelate, for 28 days. The SOD activity in the rheumatoid arthritis group increased 21% and was at almost the same level as the healthy control group. The increased activity was statistically significant.

Although copper has been viewed as the key factor in the copper/zinc SOD antioxidant defense levels, zinc plays a stabilizing role. Additionally, changes in copper and zinc status in diabetics leads to a malfunction of the copper/zinc SOD antioxidant defense system, resulting in the cardiovascular complications and retinopathy (inflammation damage to the retina of the eye) that are commonly associated with diabetes.

Albion’s patented copper, zinc, and manganese bisglycinate chelates are the trace minerals of choice when looking for a way to formulate an overall nutritional antioxidant program. They are scientifically tested, proven to be better absorbed than other mineral sources, and gentle on the body’s system.v


  1. i Henning, B., “Dietary Fat and Micronutrients: Relationships to Atherosclerosis”, The Journal of Optimal Nutrition 1 (1): 21-23, 1992.
  2. Rosenber, I., “Mutations in the Copper and Zinc Containing Superoxide Dismutase Gene are Associated with Lou Gehrig’s Disease”, Nutrition Reviews 51 (8): 243-45, August, 1993.
  3. Harman, D., “Free Radical Theory of Aging: The Free Radical Disease”, Age, 7: 111-31, 1984.
  4. Halliwell, B. and Gutteridge, JML, “Free Radicals in Biology and Medicine”, Clarendon Press, Oxford, 1985.
  5. Sato, K., Niki, E., and Shimasaki, H., “Free Radical Mediated Chain Oxidation of Low Density Lipoprotein and its Synergistic Inhibition of Vitamin E and Vitamin C”, ArchBioChem Biophys 279: 402-05, 1990.
  6. Jacques, P.F., et al., “Antioxidant Status in Persons With and Without Senile Cataracts”, Arch Opth 106: 337-40, 1988.
  7. Simin, N.M., et al., “Vitamin E Supplementation Enhances Cell Mediated Immunity in Healthy Elderly Subjects”, Am J Clin Nutr, 52: 557-63, 1990.
  8. Oberly, L.W., “Superoxide Dismutase Volume I”, CRC Press, Boca Raton, FL., 1982.ii Davis, C.D., and Gregger, J.L., Am J Clin Nutr 1992: 55: 747-52.
  9. iii Bales, C.W., et al., J Am Col Nutr 1993, p. 591.
  10. iv Kropp, J.R., “The Role of Copper in Beef Cattle Fertility.” In Ashmead, H.D., Ed The Role of Amino Acid Chelates in Animal Nutrition (Park Ridge: Noyes) 154, 1993.v DiSilvestro, R., et al., “Effects of Copper Supplementation on Ceruloplasmin and Copper-Zinc Superoxide Dismutase in Free Living Rheumatoid Arthritis Patients”, J Amer Col Nutr II (2): 177-80, 1992.
  11. David, C.D., and Greger, J.L., “Longitudinal Changes of Manganese-Dependent Superoxide Dismutase and Other Indexes of Manganese and Iron Status in Women”, Am J Clin Nutr 55: 747-52, 1992.
  12. Walter, R.M., et al., “Copper, Manganese, and Magnesium Status and Complications of Diabetes Mellitus”, Diabetes Care 14 (11) 1050-55, Nov. 1991.